Maternal genital tract infections have been associated with the development of premature rupture of the membranes (PROM) and preterm labor. It has been suggested that infection triggers a cytokine cascade that participates in the pathogenesis of PROM. Recently, we demonstrated the overexpression of matrix metalloproteinases (MMPs) in human amnion-derived cells induced by tumor necrosis factor (TNF-`). Increased expression of MMPs in chorioamnion has been proposed as a mechanism of PROM. Three pregnant rhesus monkeys were chronically catheterized at day 120 of gestation. Infection was established by inoculation of group B streptococci through a choriodecidual catheter. Amniotic fluid (AF) samples were collected serially before and after bacterial inoculation. Samples were analyzed by gel-substrate zymography and Western blot. A 92 kDa inactive form and 83 kDa active MMP-9 appeared in amniotic fluid 24 hr following infection. The amount/activity of 92 and 83 kDa forms showed a dependance on the inoculum dose and was higher when bacteria were present in amniotic fluid. Presence of high molecular weight dimers was characteristic of infection-initiated MMP-9 induction. The levels of 72 kDa type-IV collagenase (MMP-2) and tissue inhibitor of metalloproteinases (TIMP-1) were not modified by infection. These findings support the existence of a molecular link between intraamniotic infection and PROM. Presence of intrauterine infection and increased amniotic fluid cytokines correlates with higher amounts of MMP-9. Augmented extracellular matrix degradation will condition chorioamnion weakening and eventually the appearance of PROM.